Mindfulness-Based Cognitive Therapy Improves …...Please cite this article as: Willoughby B. Britton, et al., Mindfulness-Based Cognitive Therapy Improves Emotional Reactivity to

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Behavior Therapy xx (2011) xxx–xxxwww.elsevier.com/locate/bt

BETH-00324; No of Pages 16; 4C:

Mindfulness-Based Cognitive Therapy Improves EmotionalReactivity to Social Stress: Results from a Randomized

Controlled Trial

Willoughby B. BrittonWarren Alpert Medical School at Brown University

Ben ShaharOhad Szepsenwol

Interdisciplinary Center Herzliya

W. Jake JacobsUniversity of Arizona

The high likelihood of recurrence in depression is linked to aprogressive increase in emotional reactivity to stress (stresssensitization). Mindfulness-based therapies teach mindful-ness skills designed to decrease emotional reactivity in theface of negative affect-producing stressors. The primary aimof the current study was to assess whether Mindfulness-Based Cognitive Therapy (MBCT) is efficacious in reducingemotional reactivity to social evaluative threat in a clinicalsample with recurrent depression. A secondary aim was toassess whether improvement in emotional reactivity medi-ates improvements in depressive symptoms. Fifty-twoindividuals with partially remitted depression were random-ized into an 8-week MBCT course or a waitlist controlcondition. All participants underwent the Trier Social Stress

Funding for this study was provided by grants T32-AT001287,MH067553-05 and K23 AT006328-01A1 from National Institutesof Health, the Mind and Life Institute, the American Association forUniversity Women grant, and Philanthropic Educational Organi-zation (Willoughby Britton) the Lenz and Hershey Foundations andthe Brown University Contemplative Studies Initiative; the sponsorshad no further role in study design; in the collection, analysis, andinterpretation of data; in the writing of the report; and in thedecision to submit the paper for publication. This was not anindustry-supported study. The authors have indicated no financialconflicts of interest.

Address correspondence to Willoughby B. Britton, Ph.D.,Department of Psychiatry and Human Behavior, Warren AlpertMedical School at Brown University, 185 Brown Street, Providence,RI 02906; e-mail: [email protected]/xx/xxx-xxx/$1.00/0© 2011 Association for Behavioral and Cognitive Therapies. Published byElsevier Ltd. All rights reserved.

Please cite this article as: Willoughby B. Britton, et al., Mindfulness-BaStress: Results from a Randomized Controlled Trial, Behavior Therapy

Test (TSST) before and after the 8-week trial period.Emotional reactivity to stress was assessed with theSpielberger State Anxiety Inventory at several time pointsbefore, during, and after the stressor. MBCT was associatedwith decreased emotional reactivity to social stress, specif-ically during the recovery (post-stressor) phase of the TSST.Waitlist controls showed an increase in anticipatory (pre-stressor) anxiety that was absent in the MBCT group.Improvements in emotional reactivity partially mediatedimprovements in depressive symptoms. Limitations includesmall sample size, lack of objective or treatment adherencemeasures, and non-generalizability to more severely de-pressed populations. Given that emotional reactivity tostress is an important psychopathological process underly-ing the chronic and recurrent nature of depression, thesefindings suggest that mindfulness skills are important inadaptive emotion regulation when coping with stress.

Keywords: depression; emotional reactivity;meditation;Mindfulness-Based Cognitive Therapy; Trier Social Stress Test

MAJOR DEPRESSIVE DISORDER (MDD) is a debilitatingmood disorder that affects almost 19 million adultsin the United States at any given time (Narrow,1998) and almost 20% of the U.S. population overa lifetime (Blazer, Kessler, McGonagle, & Swartz,1994; Kessler, Chiu, Demler, Merikangas, &Walters, 2005). MDD is recurrent and progressive,with the likelihood of repeated episodes increasing

sed Cognitive Therapy Improves Emotional Reactivity to Social(2011), 10.1016/j.beth.2011.08.006

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with each subsequent episode. Approximately 60%of individuals who had experienced one episodewill experience a second episode, whereas 90% ofthose who had experienced three episodes will havea fourth one (Judd, 1997; Mueller et al., 1999;Solomon et al., 2000). Thus, depression modelsattempt to explain not only why certain individualsare more likely to become depressed but also whythe likelihood of recurrence increases with eachsubsequent episode (Hammen, 2005; Kendler,Thornton, & Gardner, 2000; Mitchell, Parker,Gladstone, Wilhelm, & Austin, 2003; Post, 2010;Segal, Gemar, &Williams, 1999; Segal et al., 2006;Segal, Williams, Teasdale, & Gemar, 1996).Most theories posit an interaction between a

latent but progressive vulnerability (diathesis) andnegative life events (stress; Abramson et al., 1999;Beck, 1987; Hankin, 2008; Hankin & Abramson,2001). The relationship between depression andstress is complex and changes over time, such thatearlier episodes are more likely than later episodesto be cued by major life stressors (Post, 1992;Stroud, Davila, & Moyer, 2008). Both biological(Post, 1992) and cognitive (Segal, Williams, &Teasdale, 2002) models hypothesize that individual(intrapersonal) vulnerability risk processes arestrengthened, and become more "autonomous"with each episode, such that lower levels of externalprovocation (stress) are needed to trigger a subse-quent episode. This phenomenon was first termed"kindling"1(Post, 1992) and later became knownas "stress sensitization" (Monroe & Harkness,2005; Morris, Ciesla, & Garber, 2010; Post, 2010;Stroud, Davila, Hammen, & Vrshek-Schallhorn,2011). Stress sensitization explains both the inter-and intraindividual variability in response to stress,both in terms of differing thresholds of stressneeded to trigger the same response, and differingmagnitudes of response to the same stressor.Cognitive theorists describe this progressive vulner-

ability as "cognitive reactivity,” or the activation oflatent negative information processing biases inresponse to negative affect that serve to furtherescalate the negative affect into an episode (Teasdale,1988). Biological theorists describe the diathesis asinsufficient modulation of the limbic system by theprefrontal cortex, resulting in prolonged activation ofthe amygdala and sympathetic nervous system inresponse to stressors (Davidson, Pizzagalli, Nitschke,& Putnam, 2002; Drevets, 2001; Johnstone, van

1 Increased "autonomy" in this context means "decreasedreliance on stress", but it should not be confused with the "StressAutonomy" model which states that the decoupling of stress anddepression means that stressful events are no longer capable oftriggering a depression. See Monroe and Harkness 2005.

Please cite this article as: Willoughby B. Britton, et al., Mindfulness-BStress: Results from a Randomized Controlled Trial, Behavior Therapy

Reekum, Urry, Kalin, & Davidson, 2007; Ochsner,Bunge, Gross, & Gabrieli, 2002; Ochsner & Gross,2005; Siegle, Steinhauer, Thase, Stenger, & Carter,2002; Siegle, Thompson, Carter, Steinhauer, &Thase, 2007). Both theories report the progressivepotentiation or kindling of this vulnerability, whetherdescribed in biological or cognitive terms (Post, 1992;Post, Rubinow, & Ballenger, 1984; Segal, Teasdale,Williams, & Gemar, 2002; Segal et al., 1996). Thecommon end result in both models is progressivelyprolonged or intensified negative affect or "emotionalreactivity" in response to stress, that puts individualsat risk for a depressive episode. For example, researchhas shown that heightened emotional reactivity todaily stress is a hallmark of depressive tendencies(Myin-Germeys et al., 2003; Pine, Cohen, & Brook,2001) and a predictor of future depression (Cohen,Gunthert, Butler, O'Neill, & Tolpin, 2005; Pine et al.,2001) and poor treatment response (Cohen et al.,2008). Individuals with longer durations of negativeaffect following daily life stressors are more likely todevelop depressive symptoms than those who recovermore quickly (Cohen et al., 2005). This failure to"bounce back" from transient negative affect high-lights the importance of negative affect regulation andaffect recovery in depression research and treatment.Mindfulness-based therapies such asMindfulness-

Based Stress Reduction (MBSR) and Mindfulness-Based Cognitive Therapy (MBCT) are meditation-based emotion-regulation training programs thattarget emotional reactivity to stress in awide range ofclinical and non-clinical populations. While MBSRwas created with broad clinical and non-clinicalapplications, MBCT was created by cognitivelyoriented researchers specifically for use as depressionrelapse prevention (Segal, Williams, & Teasdale,2002).MBCT assumes that among people at risk fordepression, life stress leads to dysphoria, which inturn activates negative thinking patterns, whichfurther escalate the negative affect in a cycle thatgradually progresses into a full-blown depressiveepisode (Segal, Williams, et al., 2002; Segal et al.,1996). MBCT attempts to interrupt this process byteaching depressed patients to disidentfy with or"decenter" from negative self-evaluative or rumina-tive thinking patterns and interrupt the stress-induced positive feedback loop between negativeaffect and negative thinking patterns. Thus, althoughthe associative network activated by stress includesboth negative cognitions and negative feelings(Teasdale, 1988; Teasdale, Segal, & Williams,1995), MBCT largely emphasizes and targets thecognitive reactivity component of the cognition-affect cycle (Segal, Williams, et al., 2002).In accordancewith thismodel, previous theoretical

accounts and research have focused on cognitive

ased Cognitive Therapy Improves Emotional Reactivity to Social(2011), 10.1016/j.beth.2011.08.006


3emot ional react i v i ty in mbct

reactivity as an important change process in MBCT.Cognitive reactivity is operationalized as the magni-tude of change on the Dysfunctional Attitudes Scale(Weissman, 1979) in response to negative moodprovocation or affective challenge paradigms thatare intended to serve "as manipulable experimentalanalogues for real-world environmental stressors"(Segal et al., 1999, p. 8). Segal et al. (2006) showedthat greater cognitive reactivity after cognitivebehavior therapy (CBT) or antidepressant medica-tion (ADM) predicted higher rates of relapse over thecourse of 18 months. Moreover, patients whorecovered with CBT showed significantly less cogni-tive reactivity to affective challenge than those whorecovered with ADM. Unlike CBT, MBCT aims tohelp patients hold negative thoughts (and feelings) inawareness rather diminishing them. Consistent withthis, Kuyken et al. (2010) found that individuals whohad undergone MBCT had higher cognitive reactiv-ity than those who received ADM, but the relation-ship between cognitive reactivity and relapse15 months later was decoupled in the MBCT (butnot the ADM) condition. In other words, depressedpatients undergoing MBCT responded with in-creased activation in negative thinking while in adysphoric mood, but this increase in cognitiveactivation did not result in affective deterioration.2

However, less attention has been paid to theaffective component in the cognitive-affective asso-ciative network. Emotional reactivity, or the intensityand/or duration of negative affect in response to astressor, is an important process believed to bechanged in the course of MBCT (Segal, Williams, etal., 2002). As an emotion-regulation program,MBCT teaches patients to change their relationshipswith both negative thoughts and emotions, to holdthem in awareness, and accept them with a non-judgmental and compassionate attitude, instead ofwith a secondary layer of self-referential negativeevaluation that serves to exacerbate them. Indeed,Kuyken et al. (2010) showed that developing acompassionate attitude toward one's own negativethoughts and feelings mediated the effect of MBCTon depressive symptoms and relapse. As a result, theprogram is expected to help patients regulate theiremotions more effectively in response to negativeaffect-producing stressors (Farb et al., 2007; Grant,Courtemanche, & Rainville, 2011; Segal et al.,1999). The application of MBCT in a broadersense, as an emotion-regulation intervention, is

2 On the other hand, see findings by Raes, Dewulf, VanHeeringen, &Williams (2009) which found less cognitive reactivityafter MBCT. Clearly, these inconsistent results regarding the role ofcognitive reactivity need further study but they are not the focus ofthe current study.


consistent with recent efforts to integrate cognitive,behavioral, and biological models of depression andmeditation through the study of emotion andintegrate MBCT for depression with the prevailingaffective neuroscience/emotion-regulation models ofthe larger field of mindfulness and meditationresearch (Chambers, Gullone, & Allen, 2009;Dakwar & Levin, 2009; De Raedt & Koster, 2010;Kuyken et al., 2010; Rottenberg & Johnson, 2007;Way, Creswell, Eisenberger, & Lieberman, 2010;Williams, 2010).Recently,MBCThas expanded beyond depression

relapse prevention, and also beyond depression-specific cognitive reactivity theories into broaderclinical applications and broader transdiagnosticemotion-regulation models that combine cognitive,affective, and biological approaches (Chambers etal., 2009; De Raedt & Koster, 2010; Way et al.,2010). MBCT (including the present study) hasexpanded into the treatment of acute or residualdepression (Barnhofer et al., 2009; Britton, Haynes,Fridel, & Bootzin, 2010; Eisendrath et al., 2008;Finucane&Mercer, 2006;Kenny&Williams, 2007;Kingston, Dooley, Bates, Lawlor, & Malone, 2007;Kuyken et al., 2008; Manicavasgar, Parker, &Perich, in press; Schroevers & Brandsma, 2009;Shahar, Britton, Sbarra, Figueredo, & Bootzin,2010; Williams et al., 2008), bipolar disorder(Williams et al., 2008), anxiety disorders (Evans etal., 2008; Finucane & Mercer, 2006; Kim et al.,2009; Lovas & Barsky, 2010; Piet, Hougaard,Hecksher, & Rosenberg, 2010; Schroevers &Brandsma, 2009), and conditions where emotionalreactivity and regulation (rather than depression-specific cognitive reactivity) is the common unifyingfeature and treatment target (Baer, Fischer, & Huss,2005; Foley, Baillie, Huxter, Price, & Sinclair, 2010;Oken et al., 2010; Rimes&Wingrove, 2010; Sachse,Keville, & Feigenbaum, 2011; Semple, Lee, Rosa, &Miller, 2009; van der Lee&Garssen, in press). Thus,the effects of MBCT on emotional reactivity indepression may have broad implications related tothe transdiagnostic applications ofMBCT specifical-ly and mindfulness-based interventions in general.A number of studies support the relationship

between mindfulness and reduced emotional reac-tivity to stress, including attenuated emotionalresponses to threatening situations or faster recov-ery from transient negative affect (Arch & Craske,2006, 2010; Brewer et al., 2009; Broderick, 2005;Campbell-Sills, Barlow, Brown, & Hofmann,2006; Creswell, Way, Eisenberger, & Lieberman,2007; Erisman & Roemer, 2010; Goldin &Gross, 2010; Kaviani, Javaheri, & Hatami, 2011;Kuehner, Huffziger, & Liebsch, 2009; McKee,Zvolensky, Solomon, Bernstein, & Leen-Feldner,




2007; Ortner, Kilner, & Zelazo, 2007; Pace et al.,2009; Proulx, 2008; Raes et al., 2009; Tang et al.,2007; Taylor et al., 2011; Vujanovic, Zvolensky,Bernstein, Feldner, & McLeish, 2007; Weinstein,Brown, & Ryan, 2009). For example, Arch andCraske (2006) found that undergraduate studentswho underwent a brief mindfulness induction(breath awareness) reported less negative emotionalreactivity in response to affectively valenced slidescompared to controls. Broderick (2005) found thatundergraduate students assigned to a brief mindful-ness meditation condition showed faster recoveryfrom a sad mood induction compared to adistraction condition. Decreased emotional reactiv-ity and better emotion regulation in meditators hasalso been reported using biological measures,including greater prefrontal inhibition of the amyg-dala (Brefczynski-Lewis, Lutz, Schaefer, Levinson,&Davidson, 2007; Creswell et al., 2007; Farb et al.,2007; Taylor et al., 2011; Way et al., 2010)and decreased sympathetic hyperarousal (Barnes,Treiber, & Davis, 2001; Carlson, Speca, Faris, &Patel, 2007; Maclean et al., 1994; Ortner et al.,2007; Sudsuang, Chentanez, & Veluvan, 1991).However, none of these studies examined whether

MBCT directly influences the way depressed patientsrespond emotionally to stress. In addition, thesestudies suffer from other methodological limitations:most of them used brief mindfulness induction(under 10 minutes) in undergraduate students orother non-clinical samples. Only two studies havedemonstrated improved emotional reactivity (usingpersonalized scripts) following standard (8-week)mindfulness interventions in clinical samples (socialanxiety and substance abuse; Brewer et al., 2009;Goldin&Gross, 2010), but neither used a depressedsample undergoing MBCT.Within theMBCT literature, very few studies have

examined emotional reactivity to stress. Ma andTeasdale (2004) attempted to assess MBCT's effecton stress-related relapse, butwas unable to "examinedirectly the protective effects of MBCT in the face ofdifferent severities of environmental stress becausethe occurrence of events of those who did not relapsewas not examined" (p. 39). Recently, Kaviani et al.(2011) found that MBCT reduced depression andanxiety during a natural anticipated stressor (examperiod) in a non-clinical sample of universitystudents. Thus, at present, no studies have examinedhow MBCT directly influences the way depressedpatients respond emotionally to stress.In order to most fruitfully examine MBCT's

effects on emotional reactivity to stress with specificrelevance for depression, a number of methodolog-ical issues must be considered. First, not all stressorsare equal. Segal et al. (2006) warned that the


negative mood provocation method that is typicallyused to generate negative affect (i.e., sad music ornegative slides) probably does not have theecological validity of "being rejected by a socialpartner" (p. 755). Indeed, the most salient andimpactful stressors and the ones that most com-monly precipitate depressive episodes are interper-sonal and involve social evaluation, rejection, orloss (Gunthert, Cohen, Butler, & Beck, 2007;Ingram, Miranda, & Segal, 1998; Leary, 2004).While more recent studies have recognized theimportance of using social evaluative threat as thestressor rather than a generic emotional film, scripts orslides, (Creswell et al., 2007; Pace et al., 2009;Weinstein et al., 2009), nonewere intervention studieswith clinical samples. Thus, the purpose of the presentstudy was to investigate the effects on MBCT onemotional reactivity to an ecologically valid andprovocative stressor (Trier Social Stress Test [TSST];Kirschbaum, Pirke, & Hellhammer, 1993).Second, the time course of emotional reactions

("affective chronometry") has been recently highlight-ed as important in the study of depression (Davidson,2003; Davidson, Jackson, & Kalin, 2000). Davidsonargued that "Time course variables are particularlygermane to understanding vulnerability to psychopa-thology, as certain forms of mood and anxietydisorders may be specifically associated with either afailure to turn off a response sufficiently quicklyand/or an abnormally early onset of the response”(p. 658). According to Davidson, emotional reactivityand regulation can occur at three distinct temporalwindows: before, during, and after the stressor. Forexample, he suggested less variability in emotionalreactivity during exposure to a negative affect-producing stimulus (emotion generation) and morevariability in emotional reactivity after exposure to thestimulus is terminated (emotion regulation). Studiesfrom Davidson's laboratory confirmed this by show-ing that people with different affective styles showdifferent patterns of emotional reactivity only follow-ing exposure to a negative stimulus. For example,Jackson et al. (2003) found that prefrontal cortexactivation asymmetry mostly explained variability ineyeblink startle magnitude following a negativestimulus, not during the stimulus. One notableshortcoming in such studies is the use of stimuli thatare not ecologically valid (pictures) and the short timeperiod in which reactivity was assessed (a few secondsafter exposure to the stimulus). One purpose of thecurrent study is to expand this research line byassessing emotional reactivity to a real-world stressorand by assessing reactivity during longer time periodsfollowing the stressor.To summarize, the primary aim of the current

study was to assess the effects of MBCT on emotion




reactivity in order to further clarify how MBCTworks and to expand the cognitive focus of MBCTinto a broader emotion-regulation framework. Asecondary aim was to explore whether MBCT'seffect on depressive symptoms are mediated bychanges in emotion reactivity. In addition, we soughtto address several methodological limitations thatundermined previous research on emotional reactiv-ity by (a) assessing emotion reactivity during severaltime points before, during, and after the stimulus;and (b) by using an externally valid, laboratory-based stressor that is known to provoke considerablestress. We examined our hypotheses in a waitlistrandomized controlled trial of MBCT within asample of individuals with recurrent depression.

Methodsparticipants

Participants (n=52) were recruited through com-munity advertisements for a meditation-baseddepression-relapse prevention program. Consistentwith Kuyken et al. (2008), the target population wasindividuals with a recurrent form of unipolardepression in partial or full remission with varyingdegrees of residual symptoms, as these individuals areconsidered at high risk for recurrence and becauseprevious studies have shown that MBCT is effectivefor more recurrent forms of depression (Ma &Teasdale, 2004; Teasdale et al., 2000). A StructuredClinical Interview for Axis I (SCID-I; First, 2002) andAxis II (SCID-II) Disorders and the Hamilton RatingScale for Depression (HRSD; Gelenberg et al., 1990)were used to determine diagnostic eligibility. Partic-ipants met DSM-IV criteria for major depression inthe last 5 years and had a lifetime history of at leastthree episodes, but were in partial remission duringthe last 8 weeks with a varying degree of residualsymptoms. Partial remission was defined by asubjectively reported improvement in symptoms inthe last 2 months,HRSDscore≤20 and the exclusionof severely depressed mood (HRSD item 1=>2),severe anhedonia (HRSD item 7=>3), or activesuicidal ideation (HRSD item 3=>2). Exclusioncriteria included (a) a history of bipolar disorder,cyclothymia, schizophrenia, or other psychoticdisorders, persistent antisocial behavior or repeatedself-harm, borderline personality disorder, or organ-ic brain damage; (b) current panic, obsessive-compulsive disorder, eating disorder, or substanceabuse/dependence; (c) inability to read/write inEnglish; (d) current psychotherapy; or (e) a regularmeditation practice. Individuals on antidepressantswere permitted to participate as long as they reportedno change in medication type or dose during the3 months prior to enrollment or during the activephase of the study.


procedure

All participants were recruited through communityadvertisements from January 2004 through June2005. Eligible participants participated in MBCTgroups or waitlist from July 2004 through Decem-ber 2005. Following a screening interview fordiagnostic eligibility, participants completed apacket of self-report questionnaires and a 3-hourlaboratory-based assessment that included theTSST (Kirschbaum et al., 1993).Participants were then block randomized to either

the MBCT program or waitlist control condition in a3:2 ratio without reference (stratification) to baselinecharacteristics to ensure rapid and adequate enroll-ment in the treatment arm. In blocks of five, opaque,sealed letter-size envelopes with treatment allocationinformation were shuffled and placed in identicalsequentially numbered containers and presented tothe patients after successful completion of baselineassessments. Treatment allocation was recorded bythe first author, who was also the interventiontherapist, and therefore not blind to interventionallocation. Because baseline assessments were con-ducted before randomization, participants andresearch personnel were blind to treatment condi-tions during this phase of the project. After 8 weeksof treatment or waitlist condition, participantscompleted a post-treatment questionnaire packetand returned to the laboratory to repeat the TSST.Research personnel who collected or scored any post-baseline data were also blind to treatment conditions.Waitlisted subjects entered the next available wave ofthe MBCT program, after completing the secondassessment. The sample size was calculated to have apower of .8 to detect a medium effect size for changesin depression and anxiety symptoms. A mediumeffect size has been found for depression and anxietyin two meta-analyses of MBCT/MBSR (Grossman,Niemann, Schmidt, & Walach, 2004; Hofmann,Sawyer, Witt, & Oh, 2010).The study protocol was approved by the Univer-

sity of Arizona Institutional Review Board, and allparticipants provided written informed consent forresearch participation. The study was conducted atthe University of Arizona Department of Psychol-ogy. No adverse events occurred during the trial.

laboratory-based stress-inductionprocedure

Prior to laboratory assessment, participants com-pleted 3 weeks of sleep diaries (to establish circa-dian timing). Laboratory assessments werescheduled in the late afternoon (around 5 p.m.)according to subject's circadian time becausecircadian timing affects stress reactivity (Dickerson& Kemeny, 2004). The TSST is a procedure that




reliably produces moderate psychological distressin laboratory settings (Kirschbaum et al., 1993). Inorder to prompt evaluative self-focus, subjectsdelivered a speech in front of a one-way mirrorand were told that a panel or judges were behindthe mirror, evaluating their performance. Thespeech was made in front of a microphone, undertwo tripod-mounted 1,000-watt halogen stagelights, in the presence of two video cameras withfeedback to a closed-circuit television. A judge in awhite lab coat with a clipboard was seated directlyin front of the subject and trained to give no socialfeedback. Participants were told that their perfor-mance was being recorded for later analysis.Subjects were given 5 minutes to prepare theirspeeches but were not allowed to use the notesthey had prepared. The speech lasted for a full 5minutes and was followed by a 5-minute serialsubtraction task. If the subject paused, he or shewas instructed to continue. At each laboratoryassessment (before and after the treatment period),the Spielberger State Anxiety Inventory (STAI;Spielberger, Gorsuch, Lushene, Vagg, & Jacobs,1983) was administered at five time points: (a) uponarrival in the laboratory, before the stressor(baseline); (b) immediately after the stressor withreference to anxiety levels during the stressor ("Howdid you feel DURING the speech?"); (c) immedi-ately after the stressor ("How are you feelingnow?"); (d) 40 minutes; and (e) 90 minutes post-stressor offset. These time points were based on thechronometry of psychological and physiologicalreactivity to the TSST (Dickerson & Kemeny,2004; Kirschbaum et al., 1993; Takahashi et al.,2005). Subjects were not instructed to try to alter orregulate their emotional response, althoughmany individuals will repair negative affective statesspontaneously in the absence of instruction (Forgas&Ciarrochi, 2002; Hemenover, Augustine, Shulman,Tran, & Barlett, 2008).A detailed, scripted manual of the TSST ensured

consistent administration across sessions (Payne et al.,2006). Pre- and post-treatment TSST protocolsdiffered only in the speech topic and the startingand subtraction numbers for the arithmetic task. Alllaboratory sessions were conducted by staff memberswho were blind to the treatment allocation or phaseof the study.

measures

The SCID-I (First, 2002) and the SCID-II were used toassess current and past diagnostic status at entry intothe study. In order to facilitate more accurate recallfor past depression, participantswere asked tomake alist of all past depressions andbring itwith them to theinterview. The list included age, duration, estimated


severity/impairment, and if it was associated with anidentifiable stressor. Reliability for a subset ofinterviews (10%) had over 90% agreement with anindependent clinician for the diagnosis of MDD.

Depression HistoryHistory of past depression was assessed during thediagnostic assessment. As described above, partic-ipants were asked to describe the symptom severityand duration of each possible episode. All partic-ipants had at least three prior lifetime episodes. Incases where participants were unsure about beingsufficiently symptom free between episodes toidentify distinct episodes, the number of episodeswas determined, in some instances, based on theclinical judgment of the interviewer. Additionally,some patients reported a large number of shortepisodes, whereas others reported fewer but longerepisodes. Given this ambiguity about the distinc-tiveness of episodes and the variability in number ofmonths of depression between patients, pastdepression was operationalized as the number ofmonths over the course of their lives that patientsmet diagnostic criteria for a depressive episode.

Depression SymptomsDepressive symptoms were measured with theBeck Depression Inventory (BDI; Beck, Ward,Mendelson, Mock, & Erbaugh, 1961) and theHRSD-24; Gelenberg et al., 1990). The BDI is a 21-item self-report measure that assesses depressivesymptomatology, with an emphasis on cognitivesymptoms. The BDI is a widely used measure ofdepressive symptoms and has excellent psychomet-ric properties (Beck, Steer, & Garbin, 1988; α=.81pre-treatment, .90 post-treatment).The HRSD is a widely used clinician-administered

interview assessment of depressive symptomatology(Gelenberg et al., 1990). The HRSD and diagnosticinterviews were conducted by the first author whowas trained in administering the HSRD until anadequate level of reliability (>.90)with other raters ofthe same version was achieved. The HRSD-24 wasused for screening purposes only (α=.77).

Emotional Reactivity to Social StressThe STAI-Y1 (Spielberger et al., 1983) is a 20-itemself-report inventory where respondents rate theircurrent levels of negative affect on a 4-point Likertscale, ranging from 1 (not at all) to 4 (very muchso). The STAI was initially intended to assessanxiety, but has been more recently determined tomeasure a broader type of distress, a "higher-orderfactor of negative affect" that incorporates bothanxiety (worry, distressing thoughts) and depres-sion (dysphoric mood and negative self-appraisal;Bieling, Antony, & Swinson, 1998; Caci, Bayle,




Dossios, Robert, & Boyer, 2003; Gros, Antony,Simms, & McCabe, 2007). The STAI-Y demon-strates good psychometric properties, includingstrong internal consistency (alpha coefficientsrange between .86 and .95) in diverse adult andadolescent samples, adequate test–retest reliability,and convergent validity. In the current sample,internal consistency ranged from .89 to .93 and theintraclass correlation (ICC=.93) was high. Sensi-tivity to change, as measured by effect size(ηp

2 = .44–55), and the standardized response mean(.99–1.1) for stress induction were high (seeManipulation Check section for details).

Mindfulness Meditation Practice LogsParticipants in the MBCT group kept track of theirdaily mindfulness meditation (MM) practice duringthe 8 weeks of active treatment. Diaries includedinformation about the type of meditation, thenumber of minutes practiced, and use of CD/tape.Logs for the preceding week were collected at eachclass meeting (see Britton et al., 2010, for details).

intervention

MBCT (Segal, Teasdale, & Williams, 2004; Segal,Williams, et al., 2002; Teasdale, 2004) is an 8-weekgroup-based intervention that combines principlesfrom CBT (Beck, Rush, Shaw, & Emery, 1979) andMBSR (Kabat-Zinn, 1990) using a psychoeduca-tional and client-centered format. MBCT sessionsfocus on cultivating mindfulness or non-judgmentalpresent-moment awareness of mental content andeveryday activities, including sitting, lying down,breathing, walking, and other simple movements.Homework assignments consisted of practicingMMexercises with the aid of a guided audio CD andcompleting worksheets related to stress, automaticthoughts, and common reactions to various types ofevents. A session-by-session description with hand-outs and homework assignments is available in theMBCT manual (Segal, Williams, et al., 2002).Sessions were conducted by the first author whohadmore than 10 years (approximately 3,000 hours)of mindfulness practice experience and has receivedextensive training in delivery of the program throughthe Center for Mindfulness MBSR Instructor Certi-fication Program at University of MassachusettsMedical School, and through MBCT training withDr. Zindel Segal, the first author of the MBCTmanual. Although treatment fidelity and adherencewere not formally assessed, we have previouslydemonstrated that this MBCT intervention wasefficacious in reducing residual depression symp-toms, and increasingmindfulness (MindfulAttentionAwareness Scale scores), compared to controls(Shahar et al., 2010).


statistical analysisPreliminary AnalysisBefore analysis, all variables were examined fornormality, and no outlying cases had significantinfluence on the results (as assessed by Cook'sdistance scores). Preliminary analyses were used todescribe baseline characteristics, treatment retention,and TSST manipulation checks, and to investigateany baseline group differences that might affect themain analyses.

Main AnalysisIn order to examine the effect of the treatment onanxiety levels before and after MBCT, a 2×2×5mixed-model ANOVA was performed. The between-groups factorwas treatment (MBCT, control), and thewithin-groups factors were time in relation totreatment (before treatment, after treatment) andtime in relation to the TSST (before TSST, duringthe TSST, immediately after TSST, 40 minutesafter TSST, 90 minutes after TSST). In accordancewith Hamilton and Dobson (2002), we controlledfor initial depression in all of our analyses, byentering baseline HRSD scores as a covariate. Datawere analyzed using SPSS 17.0 software. Statisticalsignificance was set at alpha levels b0.05, two-tailed. Results are reported as mean±standarderror (SE) or number/percentage unless otherwiseindicated. Effect sizes were reported as partial η2

(ηp2; small= .01, medium=.06, large= .14; Green &

Salkind, 2005).Secondary (mediational) analysis: An SPSS

Macro (Preacher & Hayes, 2008) was used inorder to examine whether improvements in anxietyregulation (emotion reactivity) mediated the effectsof MBCT on depressive symptoms. In order toconduct this analysis we first computed a meananxiety score for each participant based on his orher anxiety scores on all five assessments during theTSST. We then computed anxiety change scores bysubtracting the pre-treatment anxiety score fromthe post-treatment anxiety score. We also computeddepression change scores by subtracting pre-treatmentBDI scores from post-treatment BDI scores. Despiteconcerns that difference scores are unreliable,Rogosa and Willett (1983) showed that changescores are reliable estimates of change whenindividual differences in true change do exist.Preacher and Hayes's (2008) approach is based

on a bootstrapping procedure that extends Baronand Kenny's (1986) regression-based causal stepsapproach and the Sobel test (Sobel, 1982) for thesignificance level of indirect effect. In short, becausethe distribution of the indirect effect often deviatesfrom normality, especially in small samples(MacKinnon, Lockwood, & Williams, 2004), the




bootstrapping approach yields more accurate 95%confidence intervals for the indirect effect.

Resultsparticipant flowand sample characteristics

Of the 52 participants who completed baselineassessments, 23 were randomized to waitlist and 29to MBCT. Twenty-six (90%) MBCT and 19 (82%)waitlisted participants completed all assessments(total n=45). Of the 29 participants randomized toMBCT, three dropped out before the third class. Ofthe remaining 26, 25 (96.2%) attended at least sevenof the eight sessions, one person attended sixsessions, and all attended the all-day retreat. Figure 1displays the participants’ flowchart.

Assessed for eligibili

Enrolled (n =

Enrolled anrandomized (n =

Allocation

23 participants were allocated to wait-list group

Included in anaAnalyzed (n=19)

4 participants refused to continue due to lack of interest and scheduling conflicts

Attrition

FIGURE 1 CONSO


Sample characteristics by treatment group andcompletion status are displayed in Table 1. Treat-ment groups and completers versus non-completersdid not differ on any variable including age, sex, useof antidepressant medications, depression severity,or previous months of depression.

mm practice

Outside of class, the 27 completers reported engagingin formal MM practice an average of 39.94±10minutes/day, 5.2±1.2 days/week. According to thegoal of 45 minutes/day, 6 days/week of formal MMpractice (270 minutes/week=100%), the meanmeditation minutes across all weeks was 76±24%with a range of 79 to 308 minutes/week.

ty (n = 115)

67)

Most common reasons for exclusion were HRSD > 20 and the presence of a personality disorder

d 52)

15 individuals failed to complete all baseline assessments and were dropped before randomization

29 participants were allocated to MBCT

lysis Analyzed (n=26)

3 participants dropped from the treatment, all before the third session

RT flow diagram.


image of Figure�1


Table 1Baseline Characteristics of MBCT and Waitlist Samples

Characteristic All (n=52) Completers (n=45)

MBCT (N=29) Waitlist (N=23) MBCT (N=26) Waitlist (N=19)

Female % 79.3 87.0 76.92 94.74Age M (SE) 47.0 (1.39) 47.83 (2.28) 46.58 (1.52) 46.74 (2.68)Months depressed M 59.55 (7.10) 61.70 (8.15) 59.85 (7.88) 61.89 (8.97)On AD (%) 47.7 52.2 50.00 57.90BDI M (SE) 9.09 (1.08) 9.83 (1.27) 9.10 (1.19) 10.16 (1.4)HRSD M (SE) 10.38 (1.13) 13.17 (1.38) 10.50 (1.25) 13.32 (1.48)

Note. MBCT=Mindfulness-Based Cognitive Therapy; Months depressed=total number of months of previous depression across allepisodes; AD=antidepressant medication; BDI=Beck Depression Inventory; HRSD=Hamilton Rating Scale for Depression.

30

35

40

45

50

55

60

STA

I sc

ore

pre

post

***

** **

MBCT

30

35

40

45

50

55

60

baselinespeech

post-speech

40min

STA

I sc

ore

pre

post

*

CONTROL

during 90min

baselinespeech

post-speech

40minduring 90min

FIGURE 2 Anxiety scores pre- and post-treatment displayedseparately for controls (top) and MBCT (bottom). Note.MBCT=Mindfulness-Based Cognitive Therapy; STAI=SpielbergerState Anxiety Inventory; TSST=Trier Social Stress Test; Base-line= immediately prior to the TSST; During speech=anxiety levelwhile the TSST was occurring; Post-speech=anxiety level atthe conclusion of the TSST; 40 min.=anxiety level approximately40 minutes after the TSST had concluded; 90 min.=anxietylevel approximately 90 minutes after the TSST had concluded.*** pb .005, ** pb .01, * pb .05.


manipulation check: tsst reliably inducesnegative affect

We conducted a series of analyses to evaluate theeffectiveness of the TSST in producing negativeaffect/anxiety, and to assess whether repeatedadministration led to an attenuated response (i.e.,habituation). Using the change between baselineand the report of anxiety during the speech, theTSST produced a significant increase in anxiety forall participants at both pre-, t(44)=7.5, pb .001,ηp2= .55, and post-treatment, t(44)=5.9, pb .001,

ηp2= .44. There was no attenuation in the peak level

of anxiety produced by the TSST from pre- to post-treatment assessment (STAI score during speech atpre-treatment=53.4±10.9, at post-treatment=50.7±11.12, time main effect, F(42)=2.3, p=.14).

main analyses: the effect of thetreatment on emotional reactivityto social stress

The ANOVA failed to find a significant three-wayinteraction between treatment group, time inrelation to treatment, and time in relation to task,indicating that the trajectory of anxiety scores overtime was similar in both MBCT and control groups(see Figure 2).However, a significant two-way interaction

between treatment and time in relation to treatmentwas found, F(1, 42)=6.20, pb .05, ηp

2 = .13. Simpleeffects analyses showed that whereas averageanxiety rates (collapsing across time in relation totask) decreased in the MBCT group, they did notdecrease in the control group (see Table 2).In order to further understand the exact manner

in which MBCT decreased anxiety rates, thedifference between pre-treatment anxiety andpost-treatment anxiety was examined at eachTSST time point for the MBCT group and thecontrol group separately. In the control group, asignificant increase in pre-speech anxiety wasfound, followed by non-significant differences at


each other measurement points. In contrast, in theMBCT group, no difference was found in pre-speech anxiety and anxiety during the speech, butsignificant decreases in anxiety rates were recordedat each of the other three post-speech measurementpoints. Means and F values are presented inTable 2.


image of Figure�2


Table 2Mean (SE) Anxiety Levels Before, During, Immediately After, 40 Minutes After, and 90 Minutes After the TSST, as a Function of theTime of Measurement (Pre- or Post-treatment) and the Type of Treatment (MBCT, Control)

MBCT Control

Pre-Tx Post-Tx F(1, 42) Pre-Tx Post-Tx F(1, 42)

Baseline 40.77(1.54)

40.39(1.80)

0.05 41.40(1.90)

46.02(2.22)

4.78*

During speech 52.88(2.24)

49.53(2.13)

3.01 54.07(2.75)

52.37(2.62)

0.51

Post-speech 45.72(2.02)

37.92(1.80)

28.36*** 46.92(2.48)

45.02(2.21)

0.87

40 min. 40.94(1.96)

35.44(1.52)

11.19** 42.09(2.41)

40.89(1.87)

0.35

90 min. 38.55(2.07)

34.46(1.88)

8.34** 40.95(2.54)

42.63(2.31)

0.94

Overall 43.77(1.60)

39.55(1.53)

13.57*** 45.04(1.96)

45.39(1.89)

0.06

Note. MBCT=Mindfulness-Based Cognitive Therapy; TSST=Trier Social Stress Test; Pre-Tx=before treatment (week 0); Post-Tx=aftertreatment (week 9); Baseline= immediately prior to the TSST; During speech=anxiety level while the TSST was occurring; Post-speech=anxiety level at the conclusion of the TSST; 40 min.=anxiety level approximately 40 minutes after the TSST had concluded;90 min.=anxiety level approximately 90 minutes after the TSST had concluded. *** pb .005, ** pb .01, * pb .05.


secondary mediational analysis

The effect of treatment on change in depression(c path) was significant (β=−.42, pb .01). Inaddition, the effect of treatment on change in anxiety(a path) wasmarginally significant (β=−.27, p=.07),and the direct effect of change in anxiety on change indepression (b path) was significant (β=.39, pb .01).When change in anxiety was taken into account, thedirect effect of treatment on depression (c' path)decreased in relation to the overall effect (c path),although it stayed significant (β=−.31, pb .05).Bootstrapped .95 confidence intervals for the medi-ated effect did not include zero, indicating that theindirect effect of MBCT on depressive symptomsthrough changes in anxiety was significant. Overall,the results suggested that improvements in anxietyregulation reliably (although partially) mediated theeffects of MBCT on depressive symptoms.

DiscussionThis study assessed the effects ofMBCT on emotionalreactivity to a laboratory-based social evaluativethreat in a sample with partially remitted recurrentdepression. The main results were the following:MBCT was associated with an overall decrease inemotional reactivity. Overall anxiety levels (collapsedacross all TSST time points) decreased significantly fortheMBCTgroup, but not controls,when compared topre-treatment levels. A closer examination of specificassessment points during the TSST revealed that thisdecreased emotional reactivity in the MBCT groupwas specific to the post-stressor recovery phase. TheMBCT group showed an attenuation of negativeaffect/anxiety at all post-stressor time points com-


pared to pre-treatment baseline, whereas post-speechanxiety levels did not change from pre-treatmentamong participants in the control group. Beforetreatment, anxiety levels in all participants remainedelevated following the speech, and did not return topre-speech baseline levels until 40 minutes after thespeech had concluded. After treatment, anxiety levelsin the MBCT group returned to baseline levelsimmediately after the speech had concluded (i.e., 40minutes earlier than before treatment). These datasuggest thatMBCT training is associated with a fasteraffective recovery from potent negative affect-produc-ing stressors. Furthermore, the mediational analysisshowed that MBCT's positive effects on depressivesymptoms was partially mediated by these improve-ments in anxiety regulation.Examination of the pre-stressor time point (i.e.,

anticipatory anxiety before the speech) also suggests abeneficial effect of MBCT participation. The controlgroup showed an increase in pre-speech anxiety atpost-treatment compared to pre-treatment, whichindicates an increased sensitization to stress in thecontrol group in the formofmore anticipatory anxiety(i.e., larger emotional response to same stressor). TheMBCT group experienced similar levels of pre-speechanxiety before and after treatment, that is, they did notexperience stress sensitization that the control partic-ipants experienced. These findings suggest thatMBCTmay help depressed patients to better regulate theiranticipatory anxiety before anticipated stressors. Webelieve that the findings regarding better regulation ofanticipatory anxiety are particularly important be-cause anticipatory anxiety affects the intensity ofresponse to subsequent stressors and plays an




important role in anxiety disorders (Grillon, Ameli,Foot, & Davis, 1993) and mortality risk (Peterson,Seligman, Yurko, Martin, & Friedman, 1998).Although MBCT was associated with an overall

decrease in stress-related anxiety, these changes werespecific to pre- and post-stressor anxiety and notanxiety during the stressor. Similarly, other studies(Farb et al., 2010; Kuyken et al., 2010) also found nodifference in the magnitude of immediate emotionalresponse to provocation following 8 weeks of mind-fulness training or control treatment. Rather, in-creased duration of negative affect following astressor, rather than the initial intensity, is associatedwith depression risk (Cohen et al., 2005; Gillihan etal., 2010). Similarly, Jackson et al. (2003) found thatan affective style characteristic of depression (less left-side activation in the prefrontal cortex) was associatedwith increased emotion reactivity after picture presen-tation but not during picture presentation. This isconsistent with the idea that emotional reactions tostress, including negative affect and physiologicalarousal, are adaptive (up to a point) and need not beeliminated (Mayne, 2001; McEwen & Seeman,1999). Rapid recovery after the stressor has passedis also adaptive, as prolonged arousal and negativeaffect can deplete the organism's resources andincrease risk for depression. Our data suggest thatmindfulness trainingmay exert a nuanced effect that isspecific to the horizontal time course (chronometry)rather than a generalized suppression or blunting ofthe intensity or amplitude of emotional responses(Taylor et al., 2011).These data have clinical relevance for the treatment

of depression specifically, for the treatment of con-ditionswhere poor affect regulation is a central target(addictions), and for mindfulness and meditation-based interventions in general. In depression, thepotentiation or prolongation of negative affect, whichmay be indicative of poor prefrontal control of theamygdala, and/or activation of negative cognitiveschemas (cognitive reactivity; De Raedt & Koster,2010) is associated with higher likelihood of currentand future depression as well as poor treatmentresponse (Cohen et al., 2005, 2008; Myin-Germeyset al., 2003; Pine et al., 2001) and is therefore a centraltreatment target. Our data suggests that MBCT caneffectively target such reactivity and that this effect atleast partially mediates improvement in residualdepressive symptoms that reliably predicts relapse.In addition to depression, a broad range of

emotional disturbances characterized by persistentnegative affect are associated with poor emotionalregulation, high emotional reactivity, and/or poorprefrontal control (Baxter et al., 1989; Bench,Friston, Brown, Frackowiak, & Dolan, 1993;Clark, Chamberlain, & Sahakian, 2009;


Couyoumdjian et al., 2009; Hemenover, 2003;Mayberg et al., 1999; Meyer et al., 2004; Siegle &Hasselmo, 2002). It has been proposed that thebroad therapeutic effects of mindfulness meditationare mediated by strengthening prefrontal attentionand emotion-regulation systems (Chambers et al.,2009; Creswell et al., 2007; Davidson& Lutz, 2008;Hofmann & Asmundson, 2008; Teasdale et al.,1995; Way et al., 2010). Davidson (2003) hypoth-esized that the greater prefrontal control of theamygdala (Brefczynski-Lewis et al., 2007; Creswellet al., 2007; Farb et al., 2007; Goldin&Gross, 2010;Taylor et al., 2011; Way et al., 2010), or thedecoupling from self-referential elaboration (Farbet al., 2007, 2010; Grant et al., 2011; Taylor et al.,2011) would result in greater capacity to regulatenegative emotion and specifically "to decrease theduration of negative affect once it arises" (p. 662), inother words, hasten affective recovery.

Excessive identification with the negative emotion should resultin a perseveration or lingering of the negative affect, followingthe offset of the acute elicitor. We might thus expect that thelargest temporal region during which a transformation in theaffective reaction might occur is in the post-stimulus recoveryperiod following the offset of a negative stimulus. In otherwords,meditation training should speed the recovery following theoffset of a negative stimulus. (Davidson, 2010, p. 10).

The findings from this study add to the growingsupport for these emotion-regulation models ofmindfulness, and integrate MBCT for depressionwithin larger affective neuroscience models ofmeditation.

strengths and limitations

This study is the first to use a potent, standardizedlaboratory-based social evaluative stressor before andafter a randomized controlled trial of MBCT in adepressed population. This study also addressedthe emotional component of MBCT's theoreticalframework, which may have broader applicationsthan a depression-specific cognitive reactivity focus.At the same time, although the current studydemonstrates that MBCT reduces emotional reactiv-ity, it does not address the mechanism of action, orhow this reduction is accomplished. It is hypothesizedthat this therapeutic target is achieved throughteaching patients to hold their thoughts and feelingsin awarenesswhile adopting a patient, compassionate,and non-judgmental attitude toward these feelings.Kuyken et al. (2010) findings that self-compassionmediates MBCT's effects on outcome support thishypothesis. Because MBCT uses a variety of medita-tive techniques, it is difficult to sort out whichtechniques are related to which outcomes, so futurestudies may also want to consider dismantling designs




(Kuyken et al., 2010; Murphy, Cooper, Hollon, &Fairburn, 2009).The present study has several other limitations,

most notably the small sample size and the limitedstatistical power. The specificity of the sample(partially remitted recurrent depression) is both astrength and a limitation: Individuals with three ormore episodes and residual symptoms represent thepopulation that most benefits from MBCT (Ma &Teasdale, 2004; Teasdale et al., 2000) as well asthose at highest risk for recurrence. However, thehigh number of exclusion criteria may limit the abilityto generalize to more severely depressed samples orother clinical populations. The use of an 8-weekmindfulness course limits the ability to speculate onthe effects of other forms ofmeditation or the effects oflonger durations of training. The classic limitations ofa waitlist control design include the possibility ofexpectancy effects and differential attrition. While theMBCT group's previously reported increase inmindfulness and improvement in depression is con-sistent with other studies where high-quality MBCTwas administered, checks on competency (Crane,Kuyken, Hastings, Rothwell & Williams, 2010) andadherence (Segal et al., 2002) should be included infuture research to ensure treatment fidelity.Because self-report measures, like the STAI, are

sensitive to bias and demand characteristics, use ofobjective measures would lend convergent validityto these findings. Furthermore, use of continuous,rather than repeated, measures would yield morefine-grained information about the time course ofaffective responding.While the current study suggeststhat MBCT decreases emotional reactivity to socialstress, the clinical significance is unknown.Given thatprolonged negative affect in response to stress is amarker of depression vulnerability (Cohen et al.,2005; Gillihan et al., 2010) and treatment response(Cohen et al., 2008; Davidson et al., 2002), futureresearch should investigate whether this decreasedemotional reactivity predicts relapse/sustainedrecovery from depression, as well as the relationshipbetween and the respective contributions of cognitiveand emotional reactivity, using appropriate designs(Kazdin, 2007; Kraemer, Kiernan, Essex, & Kupfer,2008; Kraemer, Wilson, Fairburn, & Agras, 2002).

ConclusionIn conclusion, this study suggests that mindfulnessmeditation training is associated with decreasedemotional reactivity in the face of a negative affect-producing stressor and that this improvement inemotional reactivity is at least partially responsible forthe program's effect on depressive symptoms. Byproviding evidence of faster affective recovery in a(stress-sensitive) chronically depressed sample, this


study strengthens the empirical basis for applyingmindfulness-based approaches to depressed samples,aswell as other conditionswithpoor affect regulation.

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